A vulnerable plaque is an atheromatous plaque which is particularly prone to producing sudden major problems, such as a heart attack or stroke. Generally an atheroma becomes vulnerable if it grows rapidly and has a thin cover separating it from the bloodstream inside the arterial lumen. Tearing of the cover is called plaque rupture.
An atheroma (plural: atheromata) is an accumulation and swelling (-oma) in the artery walls that are made up of cells (mostly macrophage cells), or cell debris, that contain lipids (such as cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue. In the context of heart or artery matters, atheromata are commonly referred to as atheromatous plaques.
These anatomic lesions usually begin in later childhood and progress over time. Veins may not develop atheromata, unless surgically moved to function as an artery, as in bypass surgery. The accumulation (swelling) is usually between the endothelium lining and the smooth muscle wall central region (media) of the arterial tube. While the early stages, based on gross appearance, have traditionally been termed fatty streaks by pathologists, they are not composed of adipose cells, but of accumulations of white blood cells, especially macrophages that have taken up oxidized low-density lipoprotein (LDL). After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) they are called foam cells. When foam cells die, their contents are released, which attracts more macrophages and creates an extracellular lipid core near the center to inner surface of each atherosclerotic plaque. Conversely, the outer, older portions of the plaque become more calcific, less metabolically active and more physically stiff over time.
Collectively, the process of atheroma development within an individual is called atherogenesis and the overall result of the disease process is termed atherosclerosis. Because artery walls typically enlarge in response to enlarging plaques, these plaques do not usually produce much stenosis of the artery lumen. Therefore, they are not detected by cardiac stress tests or angiography, the tests most commonly performed clinically with the goal of predicting susceptibility to future heart attack. Additionally, because these lesions do not produce significant stenoses, they are typically not considered critical and/or interventionable by interventional cardiologists, even though they may be the more important lesions for producing heart attacks.
In many cases, a vulnerable plaque has a thin fibrous cap and a large and soft lipid pool underlying the cap. These characteristics together with the usual hemodynamic pulsating expansion during systole and elastic recoil contraction during diastole contribute to a high mechanical stress zone on the fibrous cap of the atheroma, making it prone to rupture. Increased hemodynamic stress correlates with increased rates of major cardiovascular events associated with exercise, especially exercise beyond levels an individual does routinely.
The most frequent cause of a cardiac event following rupture of a vulnerable plaque is blood clotting on top of the site of the ruptured plaque that blocks the lumen of the artery, thereby stopping blood flow to the tissues the artery supplies.
Upon rupture, atheroma tissue debris may spill into the blood stream; these debris are often too large to pass on through the capillaries downstream. In this situation, the debris may obstruct smaller downstream branches of the artery resulting in temporary to permanent end artery/capillary closure with loss of blood supply, and death of the previously supplied tissues. A severe case of this can be seen during angioplasty in the slow clearance of injected contrast down the artery lumen. This situation is often termed non-reflow. Additionally, atheroma rupture may allow bleeding from the lumen into the inner tissue of the atheroma making the atheroma size suddenly increase and protrude into the lumen of the artery producing lumen narrowing or even total obstruction. Repeated atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, which creates artery stenosis.
There is an unmet need for devices and methods which remove vulnerable plaques as vulnerable plaques can cause various diseases and conditions such as heart attack and stroke.